ArticleFrontiers in cellular neuroscience2022
mito-TEMPO Attenuates Oxidative Stress and Mitochondrial Dysfunction in Noise-Induced Hearing Loss
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Calycosin Safeguards Mitochondrial Genomic Stability and Iron Homeostasis via the NRF2/NRF1-TFAM Axis to Mitigate Doxorubicin-Induced Cardiotoxicity.Antioxidants (Basel, Switzerland) · 2026Article
- Sensory decline in aging and neurodegeneration: A mitochondrial perspective.Pharmacological research · 2026Review
- Subtype-Specific Vulnerability of Spiral Ganglion Neurons in Sensorineural Hearing Loss Across the Lifespan.Brain sciences · 2026Review
- MitoTEMPO modulates trigeminal activation and mitochondrial biogenesis in a nitroglycerin-induced migraine model.Molecular biology reports · 2026Article
- Microcirculatory Dysfunction and Oxidative Stress in Sudden Sensorineural Hearing Loss: Insights From a Case-Control and Experimental Study.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- The effect of mitoTEMPO on the development of hypoxia-induced pulmonary hypertension in male mice.Physiological reports · 2026Article
- XKR8 Deletion Protects Against Noise-Induced Hearing Loss by Attenuating Apoptosis and Preserving Mitochondrial Bioenergetics in the Cochlea.Molecular neurobiology · 2026Article
- Genetic and Environmental Factors Shaping Hearing Loss: Xenobiotics, Mechanisms and Translational Perspectives.Journal of xenobiotics · 2026Review
- The herbal pair ofFrontiers in nutrition · 2026Article
- PLGA nanoparticles in otoprotection and inner ear regeneration: a new frontier in nanomedicine for hearing disorders.RSC advances · 2025Review
- Targeting Aging and Diseases Associated with Ferroptosis and Senescence Through Modulation of Iron, Oxidative Stress and Lipid Peroxidation.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidative stress and reactive oxygen species in otorhinolaryngological diseases: insights from pathophysiology to targeted antioxidant therapies.Redox report : communications in free radical research · 2025Review
- miR‑34a induces apoptosis and pyroptosis in D‑Galactose‑induced aging cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunctionInternational journal of molecular medicine · 2025Article
- Noise-Induced Hearing Loss: Overview and Future Prospects for Research on Oxidative Stress.International journal of molecular sciences · 2025Review
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Reduction in mitochondrial DNA methylation leads to compensatory increase in mitochondrial DNA content: novel blood-borne biomarkers for monitoring occupational noise.Environmental health and preventive medicine · 2025Article
- Exploring biomarkers for noise-induced hearing loss through mitochondrial DNA methylation analysis.Frontiers in pharmacology · 2025Article
- Resveratrol improved mitochondrial biogenesis by activating SIRT1/PGC-1α signal pathway in SAP.Scientific reports · 2024Article
- Altered Mitochondrial Function in MASLD: Key Features and Promising Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2024Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The excessive generation of reactive oxygen species (ROS) and mitochondrial damage have been widely reported in noise-induced hearing loss (NIHL). However, the specific mechanism of noise-induced mitochondrial damage remains largely unclear. In this study, we showed that acoustic trauma caused oxidative damage to mitochondrial DNA (mtDNA), leading to the reduction of mtDNA content, mitochondrial gene expression and ATP level in rat cochleae. The expression level and mtDNA-binding function of mitochondrial transcription factor A (TFAM) were impaired following acoustic trauma without affecting the upstream PGC-1α and NRF-1. The mitochondria-target antioxidant mito-TEMPO (MT) was demonstrated to enter the inner ear after the systemic administration. MT treatment significantly alleviated noise-induced auditory threshold shifts 3d and 14d after noise exposure. Furthermore, MT significantly reduced outer hair cell (OHC) loss, cochlear ribbon synapse loss, and auditory nerve fiber (ANF) degeneration after the noise exposure. In addition, we found that MT treatment effectively attenuated noise-induced cochlear oxidative stress and mtDNA damage, as indicated by DHE, 4-HNE, and 8-OHdG. MT treatment also improved mitochondrial biogenesis, ATP generation, and TFAM-mtDNA interaction in the cochlea. These findings suggest that MT has protective effects against NIHL via maintaining TFAM-mtDNA interaction and mitochondrial biogenesis based on its ROS scavenging capacity.
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